Sympathetic Stimulation and Otic Blood Flow

1974 ◽  
Vol 83 (1) ◽  
pp. 84-91 ◽  
Author(s):  
N. W. Todd ◽  
J. E. Dennard ◽  
A. A. Clairmont ◽  
R. T. Jackson
Keyword(s):  
Blood Flow ◽  
Temporal Bone ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Bone Blood Flow ◽  
Sympathetic Stimulation ◽  
Nasal Tissue ◽  
Norepinephrine Infusion ◽  
Cervical Sympathetic ◽  
Cervical Ganglia

The radioactive microsphere technique was used in dogs to assess the effect of sympathetic stimulation on temporal bone blood flow. The stellate, caudal cervical and superior cervical ganglia, and the vertebral and cervical sympathetic nerves were stimulated. In a large majority of the animals, stimulation had no effect on temporal bone blood flow although nasal tissue was greatly affected. In a minority of animals, a small effect was seen in temporal bone tissue. Similarly, norepinephrine infusion usually did not produce evidence of reduced blood flow in the temporal bone. It was concluded that the sympathetic innervation of otic blood vessels was not capable of controlling otic blood flow, only modulating it. A sympathetic vasospasm does not seem possible. Mention is made of the dual sympathetic innervation of the cochlea described by Spoendlin and Ross. The possible mediation of sympathetic effects in the cochlea by cyclic AMP is suggested.

Unilateral and bilateral sympathetic effects on cerebral blood flow during normocapnia

1986 ◽  
Vol 250 (3) ◽  
pp. H498-H502 ◽  
Author(s):  
D. W. Busija
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sympathetic Nerves ◽  
Sympathetic Stimulation ◽  
Bilateral Stimulation ◽  
Unilateral Effects ◽  
Unilateral Stimulation ◽  
Cervical Ganglia ◽  
Bilateral Effects ◽  
Overlapping Sets

The purposes of this study were to 1) determine the effects of unilateral and bilateral sympathetic stimulation on cerebral blood flow (CBF) during normocapnia and 2) explore the mechanism by which bilateral effects are greater than unilateral effects. In anesthesized rabbits, CBF (15-microns microspheres) and internal carotid artery blood flow (ICBF) were determined during a prestimulation period and electrical stimulation of one or both superior cervical ganglia (8 or 16 Hz, 10 V, 2 ms). Resting CBF ranged from 26 to 34 ml X min-1 X 100 g-1. Unilateral stimulation did not reduce CBF at 8 Hz, but stimulation at 16 Hz reduced ipsilateral blood flow to the cerebrum by 21 +/- 5% (n = 6 from each group). In contrast, bilateral stimulation reduced blood flow to cerebrum by 22 +/- 5 and 40 +/- 4% at 8 and 16 Hz, respectively (P less than 0.05, unilateral vs. bilateral; n = 6 for each group). Similarly, unilateral stimulation at 8 Hz did not reduce ipsilateral ICBF or affect contralateral ICBF. However, bilateral stimulation at 8 Hz reduced ICBF by 51 +/- 6% on both sides. We conclude that 1) bilateral effects of sympathetic nerves on CBF are greater than unilateral effects, and 2) this difference in response may be due to activation of two overlapping sets of sympathetic nerves and release of more neurotransmitter during bilateral sympathetic stimulation.

scholarly journals Role of Prostaglandins in Modulating Sympathetic Vasoconstriction in the Cerebral Circulation in Anesthetized Rabbits

1985 ◽  
Vol 5 (1) ◽  
pp. 17-25 ◽  
Author(s):  
David W. Busija
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Cerebral Circulation ◽  
Sympathetic Nerves ◽  
Vehicle Group ◽  
Sympathetic Stimulation ◽  
Adrenergic Antagonist ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Cervical Ganglia ◽  
G Prior

The effects of the interaction between sympathetic nerves and prostaglandins in the cerebral circulation were examined. The hypothesis tested was that inhibition of prostaglandin synthesis by indomethacin would potentiate decreases in CBF caused by sympathetic nerve stimulation. In anesthetized rabbits, following administration of either indomethacin (10 mg/kg) or vehicle, CBF was measured with 15-μm microspheres prior to stimulation and following 3–5 min of electrical stimulation (4, 8, 16 Hz) of both superior cervical ganglia. In the vehicle group, CBF was 33–42 ml/min/100 g prior to stimulation. Bilateral sympathetic stimulation reduced blood flow to the cerebrum by 12 ± 6% (mean ± SEM) (p < 0.05) at 4 Hz (n = 8), by 20 ± 4% (p < 0.05) at 8 Hz (n = 12), and 21 ± 6% (p < 0.05) at 16 Hz (n = 11). In the indomethacin group, CBF was 37–48 ml/min/100 g prior to stimulation. Bilateral stimulation decreased blood flow to the cerebrum by 7 ± 5% (NS) at 4 Hz (n = 8), by 25 ± 3% (p < 0.05) at 8 Hz (n = 6), and by 20 ± 6% (NS) at 16 Hz (n = 6). Decreases in CBF during nerve stimulation were blocked by prazosin, an α-adrenergic antagonist. In additional experiments, cerebral vascular constrictor responses to hypocapnia were found to be similar in the vehicle and indomethacin groups. This study provides evidence that sympathetic nerves can decrease CBF substantially even at low stimulation frequencies. Further, results of this study indicate that prostaglandins do not attenuate the effects of sympathetic stimulation on the cerebral circulation.

scholarly journals Regional regulation of choroidal blood flow by autonomic innervation in the rat

2000 ◽  
Vol 279 (1) ◽  
pp. R202-R209 ◽  
Author(s):  
Jena J. Steinle ◽  
Dora Krizsan-Agbas ◽  
Peter G. Smith
Keyword(s):  
Blood Flow ◽  
Sympathetic Neurons ◽  
Sympathetic Innervation ◽  
Sympathetic Stimulation ◽  
Choroidal Blood Flow ◽  
Nitric Oxide Synthase Inhibitor ◽  
Doppler Flowmetry ◽  
Cervical Sympathetic ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Regional influences of parasympathetic and sympathetic innervation on choroidal blood flow were investigated in anesthetized rats. Parasympathetic pterygopalatine neurons were activated by electrically stimulating the superior salivatory nucleus, whereas sympathetic neurons were activated by cervical sympathetic trunk stimulation and uveal blood flow was measured by laser Doppler flowmetry. Parasympathetic stimulation increased flux in the anterior choroid and nasal vortex veins but not in the posterior choroid. Vasodilation was blocked completely by the neuronal nitric oxide synthase inhibitor 1-(2-trifluoromethylphenyl)imidazole but was unaffected by atropine. Sympathetic stimulation decreased flux in all regions, and this was blocked by prazosin. Parasympathetic stimulation did not affect vasoconstrictor responses to sympathetic stimulation in the posterior choroid but attenuated the decrease in blood flow through the anterior choroid and vortex veins via a nitrergic mechanism. We conclude that sympathetic α-noradrenergic vasoconstriction occurs throughout the choroid, whereas parasympathetic nitrergic vasodilation plays a selective role in modulating blood flow in anterior tissues of the eye.

Increased activity of carotid sinus baroreceptors by sympathetic stimulation and norepinephrine

1981 ◽  
Vol 240 (4) ◽  
pp. H650-H658 ◽  
Author(s):  
E. Tomomatsu ◽  
K. Nishi
Keyword(s):  
Carotid Sinus ◽  
Sympathetic Innervation ◽  
Sympathetic Nerves ◽  
Nerve Endings ◽  
Discharge Frequency ◽  
Sympathetic Stimulation ◽  
High Concentration ◽  
Excitatory Effect ◽  
Pressure Step ◽  
Stimulation Of

Effects of electrical stimulation of sympathetic nerves to the carotid sinus on the discharge of single active baroreceptor fibers of the rabbit were examined in situ and in functionally isolated carotid sinus preparations with an intact sympathetic innervation under controlled conditions of pressure and temperature. Among 30 single units, 18 units responded to sympathetic stimulation of increasing discharge frequency. The excitatory effect of sympathetic stimulation on baroreceptor activity was not abolished by phentolamine (1 mg/kg iv or 10(-6) g/ml in perfusate). In isolated carotid sinus preparations perfused with Krebs-Henseleit solution, various pressure steps were applied to the sinus, and effects of norepinephrine (NE; 10(-9) and 10(-6) g/ml) on activity of nine single baroreceptor units were examined. In the presence of 10(-9) g/ml NE, discharge frequency of all units significantly increased at a given pressure step when compared with the control, whereas NE at a high concentration (10(-6) g/ml) did not produce significant changes in the discharge frequency. It is concluded that NE released by sympathetic nerve endings most likely acts directly on the baroreceptor nerve endings and sensitizes them.

Effect of sympathetic nerves on cerebral vessels during seizures

1979 ◽  
Vol 237 (2) ◽  
pp. H178-H184 ◽  
Author(s):  
S. M. Mueller ◽  
D. D. Heistad ◽  
M. L. Marcus
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Nerves ◽  
Brain Barrier ◽  
Blood Brain ◽  
Brain Barrier Permeability ◽  
Cervical Sympathetic ◽  
The Brain

The purpose of this study was to determine the effect of activation of sympathetic pathways during seizures on cerebral blood flow and integrity of the blood-brain barrier. We measured cerebral blood flow with microspheres and disruption of the blood-brain barrier with labeled albumin in cats. One cerebral hemisphere was denervated by cutting the superior cervical sympathetic trunk on one side. During bicuculline-induced seizures, superior cervical sympathetic nerve activity increased about threefold. Blood flow to the innervated hemibrain was significantly lower than flow to denervated hemibrain. However, in relation to the total increase in flow, this effect of nerves was minor. Blood-brain barrier permeability increased about sixfold during seizures, but there was no difference between the innervated and denervated sides of the brain. We conclude that sympathetic nerves attenuate the increase in cerebral blood flow during seizures, despite the increase in metabolism, but this effect is small. Activation of sympathetic nerves does not reduce disruption of the blood-brain barrier during seizures.

Intestinal O2 uptake during sympathetic stimulation and partial arterial occlusion

1979 ◽  
Vol 236 (5) ◽  
pp. H731-H735
Author(s):  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Arterial Occlusion ◽  
Sympathetic Nerves ◽  
Capillary Density ◽  
Sympathetic Stimulation ◽  
O2 Uptake ◽  
Diffusion Limitations ◽  
O2 Extraction ◽  
Series Of Experiments ◽  
Through Diffusion

In isolated loops of canine small bowel perfused at constant blood flow, stimulating perivascular sympathetic nerves (8--10 Hz) depressed O2 extraction and O2 uptake. Because sympathetic stimulation also decreased 86Rb extraction, the results confirmed earlier studies indicating that sympathetic stimulation closes "precapillary sphincters" and through diffusion limitations reduces the capillary-to-cell flux of oxygen. To determine if sympathetic stimulation could lower O2 uptake under more physiologic circumstances, a second series of experiments was performed during constant arterial pressure perfusion. Sympathetic stimulation reduced blood flow by about 30% in the steady phase. Oxygen extraction did not increase appreciably, so O2 uptake was also reduced. When partial arterial occlusion was used to lower the blood flow to the level that it reached during sympathetic stimulation, large increases (37%) in O2 extraction occurred so that O2 uptake remained near control levels. The results indicate that after arterial occlusion local mechanisms maintain O2 uptake by increasing O2 extraction through capillary density increases, but that this mechanism is impaired by sympathetic stimulation.

Quantitative multiregional blood flow measurements during cervical sympathetic stimulation

1977 ◽  
Vol 129 (1) ◽  
pp. 129-140 ◽  
Author(s):  
Pierre Lacombe ◽  
Anne-Marie Reynier-Rebuffel ◽  
Hubert Mamo ◽  
Jacques Seylaz
Keyword(s):  
Blood Flow ◽  
Sympathetic Stimulation ◽  
Flow Measurements ◽  
Cervical Sympathetic ◽  
Blood Flow Measurements

Catecholamines abolish vagal but not acetylcholine tone in the intact cat trachea

1987 ◽  
Vol 63 (6) ◽  
pp. 2490-2498 ◽  
Author(s):  
D. G. Baker ◽  
H. Don
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Vagal Tone ◽  
Sympathetic Nerves ◽  
Posterior Wall ◽  
Inhibitory Effect ◽  
Sympathetic Stimulation ◽  
Inhibitory Effects ◽  
Transverse Tension ◽  
Cervical Sympathetic

To obtain evidence in the airways that catecholamines inhibit cholinergic neurotransmission, we recorded transverse tension in the posterior wall of an upper tracheal segment in anesthetized cats and compared the inhibitory effect of stimulating cervical sympathetic nerves when segment contraction was evoked by endogenous acetylcholine (vagal tone) with the effect when contraction was evoked by exogenous acetylcholine applied directly to the mucosal surface of the tracheal segment (ACh tone). We found that sympathetic stimulation abolished all contraction evoked by vagal tone but reduced ACh tone by only one-half. In a second group of cats we compared the inhibitory effects of sympathetic stimulation and intravenous isoproterenol during vagal and ACh tone and also during tone evoked by exogenous 5-hydroxytryptamine (5-HT tone). Sympathetic stimulation or isoproterenol injection abolished all vagal and 5-HT tone but again reduced ACh tone by only one-half. Our results suggest that catecholamines released from sympathetic nerves or injected into the circulation completely inhibit vagal tone. This inhibition may be partially responsible for inducing relaxation in airway smooth muscle.

Activation of a cranial vasodilator pathway during seizures in rats

1986 ◽  
Vol 251 (5) ◽  
pp. H969-H975 ◽  
Author(s):  
F. M. Faraci ◽  
M. G. Motley ◽  
D. D. Heistad
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Masseter Muscle ◽  
Biceps Femoris ◽  
Sympathetic Nerves ◽  
Sympathetic Denervation ◽  
Spinal Cord Section ◽  
Vasodilator Response ◽  
Cervical Sympathetic

The purpose of this study was to determine whether seizures, which activate sympathetic nerves, also activate a vasodilator pathway to extracranial tissues of the head. Blood flow was measured with microspheres during control conditions and seizures in anesthetized, paralyzed rats. Seizures were produced by bicuculline or pentylenetetrazole. During seizures in rats with intact sympathetic nerves, blood flow to masseter muscle decreased and blood flow to tongue did not change. Following bilateral cervical sympathetic denervation or high spinal cord section, seizure produced marked increases in blood flow to masseter and tongue. These vasodilator responses, which were confined to the cephalic circulation (and were not observed in biceps femoris) were blocked by hexamethonium. The vasodilator response to seizures in masseter and tongue was not significantly attenuated after atropine. Thus seizures activate a dilator pathway to extracranial tissue of the head, sympathetic nerves limit the increase in blood flow produced by activation of the cranial dilator pathway during seizures, and vasodilatation in masseter and tongue during seizures is mediated primarily by a noncholinergic mechanism.

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